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Article ; Online: Adverse effects of acute tubular injury on the glomerulus: contributing factors and mechanisms.

Babickova, Janka / Yang, Hai-Chun / Fogo, Agnes B

2024

Abstract: The intricate relationship between tubular injury and glomerular dysfunction in kidney diseases has been a subject of extensive research. While the impact of glomerular injury on downstream tubules has been well-studied, the reverse influence of tubular ... ...

Abstract	The intricate relationship between tubular injury and glomerular dysfunction in kidney diseases has been a subject of extensive research. While the impact of glomerular injury on downstream tubules has been well-studied, the reverse influence of tubular injury on the glomerulus remains less explored. This paper provides a comprehensive review of recent advances in the field, focusing on key pathways and players implicated in the pathogenesis of tubular injury on glomerular dysfunction. Anatomical and physiological evidence supports the possibility of crosstalk from the tubule to the glomerulus, whereby various mechanisms contribute to glomerular injury following tubular injury. These mechanisms include tubular backleak, dysfunctional tubuloglomerular feedback, capillary rarefaction, atubular glomeruli, and the secretion of factors from damaged tubular epithelial cells. Clinical evidence further supports the association between even mild or recovered acute kidney injury and an increased risk of chronic kidney disease, including glomerular diseases. We also discuss potential therapeutic interventions aimed at mitigating acute tubular injury, thereby reducing the detrimental effects on glomerular function. By unraveling the complex interplay from tubular injury to glomerular dysfunction, we aim to provide insights that can enhance clinical management strategies and improve outcomes for patients with kidney disease.
Language	English
Publishing date	2024-01-08
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-023-06264-7
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Article ; Online: Oxidative Stress in the Pathophysiology of Kidney Disease: Implications for Noninvasive Monitoring and Identification of Biomarkers.

Gyurászová, Marianna / Gurecká, Radana / Bábíčková, Janka / Tóthová, Ľubomíra

Oxidative medicine and cellular longevity

2020 Volume 2020, Page(s) 5478708

Abstract: Kidney disease represents a serious global health problem. One of the main concerns is its late diagnosis, only feasible in a progressed disease state. The lack of a clinical manifestation in the early stages and the fact that the commonly measured ... ...

Abstract	Kidney disease represents a serious global health problem. One of the main concerns is its late diagnosis, only feasible in a progressed disease state. The lack of a clinical manifestation in the early stages and the fact that the commonly measured parameters of renal function are markedly reduced only during advanced stages of the disease are the main cause. Changes at the molecular level of the kidney tissue occur even before nitrogenous substances, such as creatinine and urea, start to accumulate in the blood. Renal proximal tubules contain a large number of mitochondria and are critical for the energy-demanding process of reabsorption of water and solutes. Mitochondria are the largest producers of oxygen radicals, which, in turn, increase the susceptibility of kidneys to oxidative stress-induced damage. Free radicals and prooxidants produced during acute or chronic kidney injury may further aggravate the course of the disease and play a role in the pathogenesis of subsequent complications. Prevention might be the solution in CKD, but patients are often reluctant to undergo preventive examinations. Noninvasive markers and the possibility to obtain samples at home might help to increase compliance. This review will provide an overview of the possible uses of markers of oxidative status in noninvasive biofluids in patients with renal disease.
MeSH term(s)	Acute Kidney Injury/enzymology ; Acute Kidney Injury/metabolism ; Acute Kidney Injury/physiopathology ; Animals ; Biomarkers/metabolism ; Cytokines/metabolism ; Glutathione/blood ; Humans ; Inflammation/metabolism ; Kidney Tubules, Proximal/metabolism ; Mitochondria/metabolism ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Renal Insufficiency, Chronic/enzymology ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/physiopathology ; Renal Insufficiency, Chronic/urine ; Urea/blood
Chemical Substances	Biomarkers ; Cytokines ; Reactive Oxygen Species ; Urea (8W8T17847W) ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2020-01-23
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1942-0994
ISSN (online)	1942-0994
DOI	10.1155/2020/5478708
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Article ; Online: The Effect of Melatonin on Periodontitis.

Konečná, Barbora / Chobodová, Paulína / Janko, Jakub / Baňasová, Lenka / Bábíčková, Janka / Celec, Peter / Tóthová, Ľubomíra

International journal of molecular sciences

2021 Volume 22, Issue 5

Abstract: Background: Periodontitis is a chronic disease with a complex etiology that includes bacterial colonization, excessive inflammation, and oxidative stress. The hormone melatonin has antioxidant properties and might contribute to alleviating chronic ... ...

Abstract	Background: Periodontitis is a chronic disease with a complex etiology that includes bacterial colonization, excessive inflammation, and oxidative stress. The hormone melatonin has antioxidant properties and might contribute to alleviating chronic conditions by reducing oxidative stress. The aim of this study was to analyze the effect of exogenous melatonin on periodontitis in an animal model of the disease as well as in patients with periodontitis. Methods: In rats with ligature-induced periodontitis, melatonin was administered in drinking water for two weeks. In the human study, patients with treatment-resistant periodontitis were asked to rinse their mouths with a solution containing melatonin or placebo every evening for two weeks. Periodontal status as well as salivary markers of oxidative stress were assessed at the end of the study. Results: Neither radiography nor μCT revealed any significant effects of melatonin on alveolar bone loss. Gum recession was the only improved macroscopic measure in rats ( Conclusion: Our results do not support the use of melatonin for the treatment of periodontitis. However, the negative outcome is limited by the short duration of the study and the chosen route of application as well as the dose of melatonin.
MeSH term(s)	Animals ; Antioxidants/pharmacology ; Biomarkers/metabolism ; Disease Models, Animal ; Humans ; Inflammation/prevention & control ; Male ; Melatonin/pharmacology ; Middle Aged ; Oxidative Stress/drug effects ; Periodontitis/drug therapy ; Periodontitis/metabolism ; Periodontitis/pathology ; Rats ; Rats, Wistar ; Saliva/drug effects ; Saliva/metabolism
Chemical Substances	Antioxidants ; Biomarkers ; Melatonin (JL5DK93RCL)
Language	English
Publishing date	2021-02-27
Publishing country	Switzerland
Document type	Journal Article ; Randomized Controlled Trial
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22052390
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Article ; Online: Dynamics of Plasma and Urinary Extracellular DNA in Acute Kidney Injury.

Jančuška, Alexander / Potočárová, Alena / Kovalčíková, Alexandra Gaál / Podracká, Ľudmila / Bábíčková, Janka / Celec, Peter / Tóthová, Ľubomíra

International journal of molecular sciences

2022 Volume 23, Issue 6

Abstract: Early and reliable markers of acute kidney injury (AKI) are essential. One such candidate marker of tissue damage is extracellular DNA (ecDNA). The aim of our present study is to describe the unknown dynamics of ecDNA in an animal model of AKI. Glycerol- ... ...

Abstract	Early and reliable markers of acute kidney injury (AKI) are essential. One such candidate marker of tissue damage is extracellular DNA (ecDNA). The aim of our present study is to describe the unknown dynamics of ecDNA in an animal model of AKI. Glycerol-induced nephropathy was used to model AKI in adult male Wistar rats (n = 93). Blood and urine samples were collected 1, 3, and 24 h after model induction. Total ecDNA and its sub-cellular origin was assessed. In the plasma, total ecDNA and nuclear ecDNA were significantly increased in the AKI group already after 1 h (160% and 270%, respectively,
MeSH term(s)	Acute Kidney Injury/chemically induced ; Animals ; Biomarkers ; DNA, Mitochondrial ; Humans ; Male ; Plasma ; Rats ; Rats, Wistar
Chemical Substances	Biomarkers ; DNA, Mitochondrial
Language	English
Publishing date	2022-03-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23063402
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Article ; Online: Pathological and therapeutic interactions between bacteriophages, microbes and the host in inflammatory bowel disease.

Babickova, Janka / Gardlik, Roman

World journal of gastroenterology

2015 Volume 21, Issue 40, Page(s) 11321–11330

Abstract: The intestinal microbiome is a dynamic system of interactions between the host and its microbes. Under physiological conditions, a fine balance and mutually beneficial relationship is present. Disruption of this balance is a hallmark of inflammatory ... ...

Abstract	The intestinal microbiome is a dynamic system of interactions between the host and its microbes. Under physiological conditions, a fine balance and mutually beneficial relationship is present. Disruption of this balance is a hallmark of inflammatory bowel disease (IBD). Whether an altered microbiome is the consequence or the cause of IBD is currently not fully understood. The pathogenesis of IBD is believed to be a complex interaction between genetic predisposition, the immune system and environmental factors. In the recent years, metagenomic studies of the human microbiome have provided useful data that are helping to assemble the IBD puzzle. In this review, we summarize and discuss current knowledge on the composition of the intestinal microbiota in IBD, host-microbe interactions and therapeutic possibilities using bacteria in IBD. Moreover, an outlook on the possible contribution of bacteriophages in the pathogenesis and therapy of IBD is provided.
MeSH term(s)	Anti-Bacterial Agents/therapeutic use ; Bacteria/drug effects ; Bacteria/virology ; Bacteriophages ; Dysbiosis ; Fecal Microbiota Transplantation ; Gastrointestinal Microbiome/drug effects ; Host-Pathogen Interactions ; Humans ; Inflammatory Bowel Diseases/diagnosis ; Inflammatory Bowel Diseases/immunology ; Inflammatory Bowel Diseases/microbiology ; Inflammatory Bowel Diseases/therapy ; Intestines/drug effects ; Intestines/immunology ; Intestines/microbiology ; Probiotics/therapeutic use
Chemical Substances	Anti-Bacterial Agents
Language	English
Publishing date	2015-10-28
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2185929-2
ISSN	2219-2840 ; 1007-9327
ISSN (online)	2219-2840
ISSN	1007-9327
DOI	10.3748/wjg.v21.i40.11321
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Article ; Online: Glomerular proteomic profiling reveals early differences between preexisting and de novo type 2 diabetes in human renal allografts.

Kipp, Anne / Marti, Hans-Peter / Babickova, Janka / Nakken, Sigrid / Leh, Sabine / Halden, Thea A S / Jenssen, Trond / Vikse, Bjørn Egil / Åsberg, Anders / Spagnoli, Giulio / Furriol, Jessica

BMC nephrology

2023 Volume 24, Issue 1, Page(s) 254

Abstract: Background: Diabetes mellitus (DM), either preexisting or developing after transplantation, remains a crucial clinical problem in kidney transplantation. To obtain insights into the molecular mechanisms underlying PTDM development and early glomerular ... ...

Abstract	Background: Diabetes mellitus (DM), either preexisting or developing after transplantation, remains a crucial clinical problem in kidney transplantation. To obtain insights into the molecular mechanisms underlying PTDM development and early glomerular damage before the development of histologically visible diabetic kidney disease, we comparatively analysed the proteome of histologically normal glomeruli from patients with PTDM and normoglycaemic (NG) transplant recipients. Moreover, to assess specificities inherent in PTDM, we also comparatively evaluated glomerular proteomes from transplant recipients with preexisting type 2 DM (T2DM). Methods: Protocol biopsies were obtained from adult NG, PTDM and T2DM patients one year after kidney transplantation. Biopsies were formalin-fixed and embedded in paraffin, and glomerular cross-sections were microdissected. A total of 4 NG, 7 PTDM and 6 T2DM kidney biopsies were used for the analysis. The proteome was determined by liquid chromatography-tandem mass spectrometry. Relative differences in protein abundance and significantly dysregulated pathways were analysed. Results: Proteins involved in cell adhesion, immune response, leukocyte transendothelial filtration, and cell localization and organization were less abundant in glomeruli from PTDM patients than in those from NG patients, and proteins associated with supramolecular fibre organization and protein-containing complex binding were more abundant in PTDM patients. Overall, proteins related to adherens and tight junctions and those related to the immune system, including leukocyte transendothelial migration, were more abundant in NG patients than in transplanted patients with DM, irrespective of the timing of its development. However, proteins included in cell‒cell junctions and adhesion, insulin resistance, and vesicle-mediated transport were all less abundant in PTDM patients than in T2DM patients. Conclusions: The glomerular proteome profile differentiates PTDM from NG and T2DM, suggesting specific pathogenetic mechanisms. Further studies are warranted to validate these results, potentially leading to an improved understanding of PTDM kidney transplant pathophysiology and to the identification of novel biomarkers.
MeSH term(s)	Adult ; Humans ; Kidney Transplantation ; Diabetes Mellitus, Type 2 ; Proteome ; Proteomics ; Kidney ; Diabetic Nephropathies ; Allografts
Chemical Substances	Proteome
Language	English
Publishing date	2023-08-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2041348-8
ISSN	1471-2369 ; 1471-2369
ISSN (online)	1471-2369
ISSN	1471-2369
DOI	10.1186/s12882-023-03294-z
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Article: Plasma Concentrations of Extracellular DNA in Acute Kidney Injury.

Homolová, Jordanka / Janovičová, Ľubica / Konečná, Barbora / Vlková, Barbora / Celec, Peter / Tóthová, Ľubomíra / Bábíčková, Janka

Diagnostics (Basel, Switzerland)

2020 Volume 10, Issue 3

Abstract: Current diagnostic methods of acute kidney injury (AKI) have limited sensitivity and specificity. Tissue injury has been linked to an increase in the concentrations of extracellular DNA (ecDNA) in plasma. A rapid turnover of ecDNA in the circulation ... ...

Abstract	Current diagnostic methods of acute kidney injury (AKI) have limited sensitivity and specificity. Tissue injury has been linked to an increase in the concentrations of extracellular DNA (ecDNA) in plasma. A rapid turnover of ecDNA in the circulation makes it a potential marker with high sensitivity. This study aimed to analyze the concentration of ecDNA in plasma in animal models of AKI. Three different fractions of ecDNA were measured-total ecDNA was assessed fluorometrically, while nuclear ecDNA (ncDNA) and mitochondrial DNA (mtDNA) were analyzed using quantitative real-time PCR. AKI was induced using four different murine models of AKI-bilateral ureteral obstruction (BUO), glycerol-induced AKI (GLY), ischemia-reperfusion injury (IRI) and bilateral nephrectomy (BNx). Total ecDNA was significantly higher in BUO (
Language	English
Publishing date	2020-03-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662336-5
ISSN	2075-4418
ISSN	2075-4418
DOI	10.3390/diagnostics10030152
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Article ; Online: Proteomic analysis unveils Gb3-independent alterations and mitochondrial dysfunction in a gla

Elsaid, Hassan Osman Alhassan / Rivedal, Mariell / Skandalou, Eleni / Svarstad, Einar / Tøndel, Camilla / Birkeland, Even / Eikrem, Øystein / Babickova, Janka / Marti, Hans-Peter / Furriol, Jessica

Journal of translational medicine

2023 Volume 21, Issue 1, Page(s) 591

Abstract: Background: Fabry disease (FD) is a rare lysosomal storage disorder caused by mutations in the GLA gene, resulting in reduced or lack of α-galactosidase A activity. This results in the accumulation of globotriaosylceramide (Gb3) and other ... ...

Abstract	Background: Fabry disease (FD) is a rare lysosomal storage disorder caused by mutations in the GLA gene, resulting in reduced or lack of α-galactosidase A activity. This results in the accumulation of globotriaosylceramide (Gb3) and other glycosphingolipids in lysosomes causing cellular impairment and organ failures. While current therapies focus on reversing Gb3 accumulation, they do not address the altered cellular signaling in FD. Therefore, this study aims to explore Gb3-independent mechanisms of kidney damage in Fabry disease and identify potential biomarkers. Methods: To investigate these mechanisms, we utilized a zebrafish (ZF) gla Results: Our proteomics analysis of renal tissues from zebrafish revealed downregulation of lysosome and mitochondrial-related proteins in gla Conclusions: These results suggest that the alterations observed at the proteome and mitochondrial level closely resemble well-known GLA mutation-related alterations in humans. Importantly, they also unveil novel Gb3-independent pathogenic mechanisms in Fabry disease. Understanding these mechanisms could potentially lead to the development of innovative drug screening approaches. Furthermore, the findings pave the way for identifying new clinical targets, offering new avenues for therapeutic interventions in Fabry disease. The zebrafish gla
MeSH term(s)	Animals ; Humans ; Antioxidants ; Fabry Disease ; Mitochondria ; Proteome ; Proteomics ; Zebrafish ; alpha-Galactosidase/metabolism
Chemical Substances	Antioxidants ; Proteome ; alpha-Galactosidase (EC 3.2.1.22)
Language	English
Publishing date	2023-09-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2118570-0
ISSN	1479-5876 ; 1479-5876
ISSN (online)	1479-5876
ISSN	1479-5876
DOI	10.1186/s12967-023-04475-y
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Article ; Online: Cell-free DNA: the role in pathophysiology and as a biomarker in kidney diseases.

Celec, Peter / Vlková, Barbora / Lauková, Lucia / Bábíčková, Janka / Boor, Peter

Expert reviews in molecular medicine

2018 Volume 20, Page(s) e1

Abstract: Cell-free DNA (cfDNA) is present in various body fluids and originates mostly from blood cells. In specific conditions, circulating cfDNA might be derived from tumours, donor organs after transplantation or from the foetus during pregnancy. The analysis ... ...

Abstract	Cell-free DNA (cfDNA) is present in various body fluids and originates mostly from blood cells. In specific conditions, circulating cfDNA might be derived from tumours, donor organs after transplantation or from the foetus during pregnancy. The analysis of cfDNA is mainly used for genetic analyses of the source tissue -tumour, foetus or for the early detection of graft rejection. It might serve also as a nonspecific biomarker of tissue damage in critical care medicine. In kidney diseases, cfDNA increases during haemodialysis and indicates cell damage. In patients with renal cell carcinoma, cfDNA in plasma and its integrity is studied for monitoring of tumour growth, the effects of chemotherapy and for prognosis. Urinary cfDNA is highly fragmented, but the technical hurdles can now be overcome and urinary cfDNA is being evaluated as a potential biomarker of renal injury and urinary tract tumours. Beyond its diagnostic application, cfDNA might also be involved in the pathogenesis of diseases affecting the kidneys as shown for systemic lupus, sepsis and some pregnancy-related pathologies. Recent data suggest that increased cfDNA is associated with acute kidney injury. In this review, we discuss the biological characteristics, sources of cfDNA, its potential use as a biomarker as well as its role in the pathogenesis of renal and urinary diseases.
MeSH term(s)	Biomarkers ; Cell-Free Nucleic Acids ; DNA ; Genetic Testing/methods ; Genetic Testing/standards ; Humans ; Kidney Diseases/diagnosis ; Kidney Diseases/genetics ; Kidney Diseases/metabolism ; Liquid Biopsy/methods ; Liquid Biopsy/standards ; Prognosis
Chemical Substances	Biomarkers ; Cell-Free Nucleic Acids ; DNA (9007-49-2)
Language	English
Publishing date	2018-01-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1462-3994
ISSN (online)	1462-3994
DOI	10.1017/erm.2017.12
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Article ; Online: Glomerular transcriptomics predicts long term outcome and identifies therapeutic strategies for patients with assumed benign IgA nephropathy.

Rivedal, Mariell / Mikkelsen, Håvard / Marti, Hans-Peter / Liu, Lili / Kiryluk, Krzysztof / Knoop, Thomas / Bjørneklett, Rune / Haaskjold, Yngvar Lunde / Furriol, Jessica / Leh, Sabine / Paunas, Flavia / Bábíčková, Janka / Scherer, Andreas / Serre, Camille / Eikrem, Oystein / Strauss, Philipp

Kidney international

2023 Volume 105, Issue 4, Page(s) 717–730

Abstract: Some patients diagnosed with benign IgA nephropathy (IgAN) develop a progressive clinical course, not predictable by known clinical or histopathological parameters. To assess if gene expression can differentiate between progressors and non-progressors ... ...

Abstract	Some patients diagnosed with benign IgA nephropathy (IgAN) develop a progressive clinical course, not predictable by known clinical or histopathological parameters. To assess if gene expression can differentiate between progressors and non-progressors with assumed benign IgAN, we tested microdissected glomeruli from archival kidney biopsy sections from adult patients with stable clinical remission (21 non-progressors) or from 15 patients that had undergone clinical progression within a 25-year time frame. Based on 1 240 differentially expressed genes from patients with suitable sequencing results, we identified eight IgAN progressor and nine non-progressor genes using a two-component classifier. These genes, including APOL5 and ZXDC, predicted disease progression with 88% accuracy, 75% sensitivity and 100% specificity on average 21.6 years before progressive disease was clinically documented. APOL lipoproteins are associated with inflammation, autophagy and kidney disease while ZXDC is a zinc-finger transcription factor modulating adaptive immunity. Ten genes from our transcriptomics data overlapped with an external genome wide association study dataset, although the gene set enrichment test was not statistically significant. We also identified 45 drug targets in the DrugBank database, including angiotensinogen, a target of sparsentan (dual antagonist of the endothelin type A receptor and the angiotensin II type 1 receptor) currently investigated for IgAN treatment. Two validation cohorts were used for substantiating key results, one by immunohistochemistry and the other by nCounter technology. Thus, glomerular mRNA sequencing from diagnostic kidney biopsies from patients with assumed benign IgAN can differentiate between future progressors and non-progressors at the time of diagnosis.
MeSH term(s)	Adult ; Humans ; Glomerulonephritis, IGA/diagnosis ; Glomerulonephritis, IGA/drug therapy ; Glomerulonephritis, IGA/genetics ; Genome-Wide Association Study ; Kidney Glomerulus/pathology ; Gene Expression Profiling/methods ; Gene Expression Regulation
Language	English
Publishing date	2023-12-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2023.12.010
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